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Hypothetical Molecular Mechanisms Underlying Hyperhomocysteinemia-Mediated Vascular Disorders Hyperhomocysteinemia-Mediated Oxidant Stress through Imbalanced Thiol Redox Status Numerous studies indicate that oxidant stress plays a role in the development of occlusive atherosclerotic lesions that are observed primarily in homozygotes for the CBS defect (McCully, 1983) and later in experimental hyperhomocysteinemia

By utilising non-traditional antimicrobial mechanisms like ROS generation and pH/enzyme-triggered release, these multifunctional platforms not only modulate dysbiosis and disrupt resilient biofilms, but they also achieve up to 90% wound closure in preclinical models

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Because the whole-cell biocatalyst required the addition of ATP, we were not able to observe the effect of the glgB deletion on GSH synthesis

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